This two-step approach eliminated resistant tumor populations, cured approximately 50% of established B16 melanomas, and generated neoantigen-specific immune responses against CSDE1P5S as well as TYRP2, a melanocyte differentiation antigen that serves as a shared self/tumor-associated antigen, indicating the induction of both neoantigen- and self-antigen-directed immunity. The gene discussed is DCT; the disease is melanoma.